The confusion surrounding whether prohormones are considered steroids stems from their similar effects and complex legal status. While chemically distinct upon ingestion, prohormones are designed to function as precursors to anabolic hormones. This difference in how the compounds become active has been the source of debate and regulatory attempts. This article clarifies the relationship between these compounds, examining their definitions, metabolic pathways, legal standing, and shared physiological consequences.
Understanding Prohormones and Anabolic Steroids
Anabolic-androgenic steroids (AAS) are synthetic derivatives of the male hormone testosterone. These substances are biologically active immediately upon entering the bloodstream, where they directly bind to androgen receptors. This maximizes muscle-building (anabolic) and male characteristic-promoting (androgenic) effects.
Prohormones, in contrast, are precursor compounds that are biologically inactive or only minimally active. They are designed to enter the body and become active only after undergoing a metabolic conversion process. The name “prohormone” literally means “before the hormone,” signifying they are one or two enzymatic steps away from being an active steroid. Prohormones must be processed by the body before they can exert the same effects as an anabolic steroid.
The Mechanism of Conversion
The transformation of an inactive prohormone into an active anabolic steroid occurs through specific enzymatic reactions within the body. After ingestion, prohormones are transported to the liver, which is the primary site for this metabolic processing. The liver contains various enzymes that normally handle the body’s natural steroid production and metabolism.
Key enzymes involved in this conversion include various isoforms of hydroxysteroid dehydrogenases (HSDs) and cytochrome P450 (CYP) enzymes. For example, a prohormone such as androstenedione can be converted into testosterone by the enzyme 17-beta hydroxysteroid dehydrogenase (17\(\beta\)-HSD). This metabolic step completes the chemical structure of the compound, turning the inert precursor into a fully functional steroid.
This enzymatic conversion makes prohormones functionally similar to steroids once they are in the body. The resulting active hormone, whether testosterone or a nandrolone derivative, then interacts with muscle cell receptors just as a traditional anabolic steroid would. This confirms that, while the compound ingested is a precursor, the compound acting on the body is an anabolic steroid.
Legal Classification and Current Regulation
The legal status of prohormones has historically been complex due to manufacturers exploiting regulatory loopholes. The US Anabolic Steroid Control Act of 2004 was an initial attempt to address this by expanding the definition of an anabolic steroid to include many prohormones, such as androstenedione. This legislation classified these compounds as Schedule III controlled substances, making their distribution and possession illegal without a prescription.
Despite the 2004 Act, manufacturers introduced new “designer” prohormones with slight chemical modifications to circumvent the existing definition. This led to the passage of the Designer Anabolic Steroid Control Act (DASCA) of 2014, which further strengthened regulations. DASCA added approximately two dozen specific compounds to the list of controlled substances and expanded the Attorney General’s authority to temporarily schedule new, chemically similar substances.
The intent of DASCA was to close the regulatory loophole by targeting the structural core of the anabolic steroid molecule. This effectively classified nearly all compounds that function as prohormones as illegal anabolic steroids. Today, the vast majority of compounds historically sold as “prohormone supplements” are illegal for sale in the United States without a prescription.
Shared Physiological Impacts
Because prohormones convert into active anabolic steroids, their practical consequences for health closely mirror those of traditional AAS. One significant concern is liver strain, or hepatotoxicity, particularly with prohormones that are 17-alpha alkylated to ensure oral bioavailability. This chemical modification makes the compound resistant to breakdown, forcing the liver to work harder to metabolize it and potentially leading to cellular damage.
Both active steroids and converted prohormones suppress the body’s natural hormone production by disrupting the Hypothalamic-Pituitary-Testicular Axis (HPTA). High levels of synthetic androgen signal the brain to stop producing its own testosterone, often leading to a temporary state of low testosterone after use is discontinued. This suppression requires a post-cycle therapy to help restore hormonal balance.
The use of these compounds also carries a risk of cardiovascular strain. Steroids and their prohormone precursors can negatively alter cholesterol profiles, increasing low-density lipoprotein (LDL) cholesterol and decreasing high-density lipoprotein (HDL) cholesterol. This change in lipid balance, coupled with potential increases in blood pressure, contributes to an elevated risk of cardiovascular problems.